Important Notice:

The Q Fever Register is moving to the Australian Immunisation Register from Monday 15 April 2024

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Registrations from Monday 15 April 2024 should be reported to the Australian Immunisation Register. Using the Australian Immunisation Register | Australian Government Department of Health and Aged Care.

Click here for the article regarding changes to the Q Fever Register

About Q Fever

Q Fever was first recognised in Australia during the 1930's when workers at a Brisbane meat processor became ill with a fever. as the cause of the illness was unknown, the workers were diagnosed with 'Query' fever. This was eventually abbreviated to Q Fever. with the possible exception of a few European countries and New Zealand, cases of Q Fever have been reported worldwide and from every State and Territory in Australia.

[This information is from the 'Q Fever Information Kit for the Australian Meat Industry' pages 4 to 7, prepared for the Meat Research Corporation (now Meat and Livestock Australia) by Julie O'Neill, 1997]

Reservoir and Livestock Infection

The organism, Coxiella burnetii, that causes Q Fever in humans can exist in a variety of domestic and wild animals without the animal displaying apparent signs of infection. In Australia C. burnetii is maintained in the wild by bush animals such as kangaroos, bandicoots and rodents and their attendant ticks. Mutually coexistent ticks may involve feral and domestic goats, cattle or sheep which in turn infect their attendant ticks. Hide, fleece or hair contamination also occurs when infected ticks shed the heavily concentrated organism in their faeces while feeding on stock.

An infected animal excretes large amounts of the organism in its urine, faeces and milk and, in high concentrations in the birth fluids, placenta, on the foetus and newly born and in the uterine discharges following the birth of young. Organisms in the placenta are particularly concentrated; one gram of placental tissue may contain one billion organisms.

The important feature of the organism is its ability to withstand harsh environmental conditions; resisting heating, drying and sunlight to survive for more than a year at 4ºC in a dried state. The organism dried on wool has been shown to remain infective for 7 to 9 months at 15ºC to 20ºC and for 12 to 16 months at 4ºC to 6ºC. Infected tick faeces has demonstrated its ability to remain infectious, in a dried state, for approximately 2 years.

The organism is highly contagious within domestic herds where infection is mostly maintained through inhalation of infected dusts and contaminated droplets liberated from the products of an infected animal. Within a few months of the organism being introduced to a herd, 80% of the stock may become infected. The infection almost invariably spreads to neighbouring stock, native and feral animals and sometimes domestic cats and dogs. Once a herd is infected, it normally remains infected.

Transmission to Humans

Infection could occur via skin abrasions and splashes of infected material into the eye. The consumption of unpasteurized milk from infected cows and goats has accounted for small numbers of Q Fever cases yet, in some instances, drinking infected raw milk has had an immunising effect in the absence of a clinical disease. Human to human infection is very uncommon as is infection from tick bites. Inhalation of the organism, as a result of direct or indirect exposure to contaminated aerosols, is the most common mechanism of human infection. 

Direct Exposure

Fine mists, or very small droplets; liberated from the blood, milk, urine, faeces, when the young are born and especially from the placenta and birth fluids of an infected animal; directly exposes humans to infected aerosols. Air samples from the vicinity of parturient animals and areas contaminated with heavily infected placentas have shown the organism will continue to be released, contaminating the environment for up to 2 weeks following the birth of young.

During the slaughter and processing of infected animals, fine mists can also be released into the air from the blood and when handling the udder, bladder, intestines and the uterus, foetus and other products of conception. Infection may also occur with exposure to contaminated water droplets or fine mists, dispersed when using high pressure hoses to wash infected material, or dust, from stock, building structures, animal transport vehicles and personal protective clothing such as boots and plastic aprons. 

The larger droplets and released infected matter can collect on the animal's hide, hair or fleece and heavily contaminate the ground or floor, surrounding area, nearby structures or machinery and such materials as straw and clothing. The lighter smaller droplets freely disperse into the air, and may be disseminated for some distance, before settling. These contaminated droplets and matter then dry to form a highly infectious dust. 

Indirect Exposure

Humans may inhale infected dust, formed from contaminated droplets and the organism-laden products from an infected animal, when it is blown (possibly for a kilometre or more) in dry and windy weather. The organism can be released into the air when handling materials, working within areas or on structures, that have been contaminated by infective dust. This dust may have collected during wind borne dissemination or as the result of direct contamination with infected products that have dried to form a dust. Moving animals in the yards, pens or holding paddocks and stock transport trucks can also raise infective dusts. 

as the organism can endure harsh conditions for many months in a dried state; either in the ground or attached to buildings, machinery, stock transport vehicles, straw, wool, hides or work clothing; it is a constant, and often hidden, source of infection. Infected dust and dried matter may also be transported on the above-mentioned materials and later, released into the air, exposing individuals outside of the recognised risk environments to infection.

Contaminated aerosols, whether they be infected dust or droplets, are considered extremely infectious. It is estimated that very small numbers of C. burnetii (possibly between one to ten organisms) are sufficient to cause Q Fever in humans.

Incubation Period

The interval between inhalation of the organism (ie. exposure) and onset of the illness may range from 14 to 60 days, depending on the intensity of exposure to the organism. Individuals exposed to the highly infective products of conception have been observed to have the shortest incubation period and the most severe illness. The usual incubation period is 19 to 21 days. 

Signs and Symptoms

These include sudden onset of acute fever, chills, profuse sweating, cough, severe headache, muscle pains and weakness. It is not unusual for a diagnosis of influenza to be made during the initial stages of the illness. as the symptoms could be the body's response to any number of invading organisms or viruses, a series of laboratory blood tests are required to confirm a diagnosis of Q Fever. 

Individual responses to this infection, as with all infections, will vary. For some, there will be no illness and a past exposure may only become apparent when antibodies are detected 'in a blood sample or there is a positive skin test reaction. Others may have symptoms for a few days, dismissing the illness as 'viral' or they could just feel 'off colour' and, as such, may not seek medical attention. 

Typically though, the fever lasts seven to ten days and is accompanied by excessive sweating (warranting many changes of clothes and bed linen), nausea, vomiting, diarrhoea, and anorexia. There is often weight loss of 6 to 12 kilograms if the acute episode is prolonged. For some, the recovery period will be protracted following an acute infection. 

On occasions, other patterns of the disease can be so debilitating that hospitalisation is required. as the organism is circulated through the body in the blood stream, any organ system can become involved including the central nervous system, lungs, liver, kidney, testes and heart muscle and tissue. Persons with pre-existing heart valve damage resulting from disease or congenital malformation could be at risk of developing endocarditis.

Death from acute Q Fever is very rare and occurs mainly in the elderly or those whose health is compromised by illness or disease. 

Generally, the illness will last one to six weeks with most patients gaining a life-long immunity to further infection. 


Appropriate antibiotics, commenced soon after the onset of the illness, is the usual therapy. 


as stated earlier, the major life-threatening complication of acute Q Fever is chronic endocarditis which may develop shortly after the acute attack but more often, does not become apparent until 2 to 4 years or even longer following the acute attack. The complication is rare; estimates vary, but a rate of around 1% of acute cases is probably realistic. 

Other complications in which the Q Fever organism can readily be demonstrated by special techniques include chronic granulomatous hepatitis, in the absence of endocarditis, and infections of the bone (osteitis). 

Women infected clinically or sub-clinically with C.burnetii, either before conception, or in early pregnancy, may experience a reactivation of infection at parturition and excrete the organism in the products of conception. Fortunately, the infection reactivation is usually without effect on mother or child, although foetal damage has been reported.

In recent years it has become apparent that there may be another different, chronic, disabling sequel to acute Q Fever which takes the form of a prolonged debility and fatigue syndrome. This sequel has features in common with the chronic fatigue syndrome thought to follow proven virus infections (eg., Ross River fever, glandular fever) or virus-like episodes in which a viral cause is not established by laboratory tests. 

Depending on the stringency of diagnostic criteria, the post Q Fever fatigue syndrome (QFS) follows about 20% of acute Q Fever cases. as it may last for 5-10 or more years the cost to the industry, occupational health insurers and Health Services is considerable. 

Patients suffer from an incapacitating fatigue on minor exertion, muscle and joint pains, headaches, profuse sweats, particularly at night, interrupted sleep patterns, altered mental concentration, volatile moods and depression, among other symptoms. Unfortunately, at present, the diagnosis depends almost entirely on the patients' account of symptoms and there are no readily available laboratory tests, such as antibody tests, to confirm the diagnosis. However, several surveys of QFS patients and controls in Australia and the United Kingdom have confirmed the existence of the syndrome as a sequel to acute Q Fever.

It should be noted that the symptoms described are common in the first six months after acute Q Fever in patients who will eventually make an uncomplicated recovery; in contrast, QFS patients are still symptomatic 3-5 years after the acute illness. Although standard clinical, physical examination and clinical pathology tests are frustratingly negative, recent research work has revealed that QFS patients have evidence of chronic dysregulation of the cellular immune system possibly resulting from a low-level persistence of the Q Fever organism or its antigens after the original acute attack. The results of this research have still to be translated into a readily available routine laboratory test to confirm the clinical diagnosis. 

Given the disabling nature of QFS, its duration, the conflicts over diagnosis, and its costs, the advantages of vaccination to prevent the condition and the other chronic sequels are self-evident.